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Background <p>Glucosylsphingosine (Lyso-GL-1), a glycosphingolipid formed by glucosylceramide hydrolysis, is known to be increased in Gaucher disease. Recently, increased ceramides and sphingolipids have been implicated in obesity, insulin resistance, and atherogenesis. However, limited data exists on serum Lyso-GL-1 level in children with obesity and its relation with insulin resistance, lipid dysfunction, and atherogenesis. Hence, this study aimed to assess Lyso-GL-1 level among children with obesity and correlate it with biomarkers of insulin resistance and atherogenic index of plasma (AIP).</p> Methodology <p>Sixty children with obesity with a mean age of 10.06 years (SDS ± 2.22) and 60 age- and sex-matched normal-weighed controls were assessed for anthropometric measures, mean blood pressure percentiles, serum Lyso-GL-1, glycated hemoglobin (HbA1c), fasting insulin, triglycerides, cholesterol, low-density (LDL-C) and high-density lipoprotein cholesterol (HDL-C) with calculation of the homeostatic model assessment of insulin resistance (HOMA-IR) and the AIP.</p> Results <p>Children with obesity have significantly higher Lyso-GL-1 and AIP than controls. Lyso-GL-1 is significantly positively correlated with body mass index (BMI) z-score, waist/hip ratio z-score, systolic and diastolic blood pressure percentiles, LDL-C, HOMA-IR, and AIP (<i>p</i> &lt; 0.05), being independently correlated with systolic blood pressure percentile, LDL-C, and AIP on multivariate regression analysis.</p> Conclusion <p>Serum Lyso-GL-1 is elevated in children with obesity, being closely correlated with hypertension, insulin resistance, and atherogenesis. This could provide a mechanistic insight on the role of Lyso-GL-1 in obesity and atherogenesis. Further studies are warranted to explore the potential role of Lyso-GL-1 as a biomarker and target for the prevention and treatment of obesity-related atherogenesis and insulin resistance.</p> <p></p>

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Elevated serum glucosylsphingosine level in children with obesity: relation to plasma atherogenesis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月22日

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  • Nouran Y. Salah,
  • Dina Abdel Hakam,
  • Fatma AbdEllah Abdullah,
  • Marwa Samir Hamza,
  • Eman Aly Ramadan,
  • Rana Mahmoud

摘要

Background

Glucosylsphingosine (Lyso-GL-1), a glycosphingolipid formed by glucosylceramide hydrolysis, is known to be increased in Gaucher disease. Recently, increased ceramides and sphingolipids have been implicated in obesity, insulin resistance, and atherogenesis. However, limited data exists on serum Lyso-GL-1 level in children with obesity and its relation with insulin resistance, lipid dysfunction, and atherogenesis. Hence, this study aimed to assess Lyso-GL-1 level among children with obesity and correlate it with biomarkers of insulin resistance and atherogenic index of plasma (AIP).

Methodology

Sixty children with obesity with a mean age of 10.06 years (SDS ± 2.22) and 60 age- and sex-matched normal-weighed controls were assessed for anthropometric measures, mean blood pressure percentiles, serum Lyso-GL-1, glycated hemoglobin (HbA1c), fasting insulin, triglycerides, cholesterol, low-density (LDL-C) and high-density lipoprotein cholesterol (HDL-C) with calculation of the homeostatic model assessment of insulin resistance (HOMA-IR) and the AIP.

Results

Children with obesity have significantly higher Lyso-GL-1 and AIP than controls. Lyso-GL-1 is significantly positively correlated with body mass index (BMI) z-score, waist/hip ratio z-score, systolic and diastolic blood pressure percentiles, LDL-C, HOMA-IR, and AIP (p < 0.05), being independently correlated with systolic blood pressure percentile, LDL-C, and AIP on multivariate regression analysis.

Conclusion

Serum Lyso-GL-1 is elevated in children with obesity, being closely correlated with hypertension, insulin resistance, and atherogenesis. This could provide a mechanistic insight on the role of Lyso-GL-1 in obesity and atherogenesis. Further studies are warranted to explore the potential role of Lyso-GL-1 as a biomarker and target for the prevention and treatment of obesity-related atherogenesis and insulin resistance.